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Acute Changes in Pulmonary Artery Pressures Due to Exercise and Exposure to High Altitude Do Not Cause Left Ventricular Diastolic Dysfunction^*

^* From the Division of Cardiology (Drs. Bernheim, Kiencke, and Brunner-La Rocca), University Hospital, Basel, Switzerland; the Intensive Care Unit (Drs. Fischler, Dorschner, Debrunner, and Maggiorini), Department of Internal Medicine, University Hospital, Zurich, Switzerland; and the Department of Sports Medicine (Dr. Mairbäurl), University Hospital, Heidelberg, Germany.

Correspondence to: Alain M. Bernheim, MD, Division of Cardiology, University Hospital, Petersgraben 4, 4031 Basel, Switzerland; e-mail: bernheima{at}uhbs.ch

Abstract

Background: Altitude-induced pulmonary hypertension has been suggested to cause left ventricular (LV) diastolic dysfunction due to ventricular interaction. In this study, we evaluate the effects of exercise- and altitude-induced increase in pulmonary artery pressures on LV diastolic function in an interventional setting investigating high-altitude pulmonary edema (HAPE) prophylaxis.

Methods: Among 39 subjects, 29 were HAPE susceptible (HAPE-S) and 10 served as control subjects. HAPE-S subjects were randomly assigned to prophylactic tadalafil (10 mg), dexamethasone (8 mg), or placebo bid, starting 1 day before ascent. Doppler echocardiography at rest and during submaximal exercise was performed at low altitude (490 m) and high altitude (4,559 m). The ratio of early transmitral inflow peak velocity (E) to atrial transmitral inflow peak velocity (A), pulmonary venous flow parameters, and tissue velocity within the septal mitral annulus during early diastole (E’) were used to assess LV diastolic properties. LV filling pressures were estimated by E/E’. Systolic right ventricular to atrial pressure gradients (RVPGs) were measured in order to estimate pulmonary artery pressures.

Results: At 490 m, E/A decreased similarly with exercise in HAPE-S and control subjects (HAPE-S, 1.5 ± 0.3 to 1.3 ± 0.3; control, 1.7 ± 0.4 to 1.3 ± 0.3; p = 0.12 between groups) [mean ± SD], whereas RVPG increased significantly more in HAPE-S subjects (20 ± 5 to 43 ± 9 mm Hg vs 18 ± 3 to 28 ± 3 mm Hg, p < 0.001). Changes in RVPG levels during exercise did not correlate with changes in E/A (p > 0.1). From 490 to 4,559 m, no correlations between changes in RVPG and changes in E/A or atrial reversal (both p > 0.1) were observed. Neither of the groups showed an increase in E/E’ from 490 to 4,559 m.

Conclusion: Increased pulmonary artery pressure associated with exercise and acute exposure to 4,559 m appears not to cause LV diastolic dysfunction in healthy subjects. Therefore, ventricular interaction seems not to be of hemodynamic relevance in this setting.

Key Words: acute pulmonary hypertension • healthy subjects • high altitude • left ventricular diastolic function

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